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. 2022 Feb 28;12(1):e12051.
doi: 10.1002/pul2.12051. eCollection 2022 Jan.

A unique gut microbiota signature in pulmonary arterial hypertension: A pilot study

Arun Jose  1 , Senu Apewokin  2 , Walaa E Hussein  2 , Nicholas J Ollberding  3   4 , Jean M Elwing  1 , David B Haslam  4
Affiliations

A unique gut microbiota signature in pulmonary arterial hypertension: A pilot study

Arun Jose et al. Pulm Circ. .

Abstract

Pulmonary arterial hypertension (PAH) is a progressive, ultimately fatal cardiopulmonary disease associated with a number of physiologic changes, which is believed to result in imbalances in the intestinal microbiota. To date, comprehensive investigational analysis of the intestinal microbiota in human subjects is still limited. To address this, we performed a pilot study of the intestinal microbiome in 20 PAH and 20 non-PAH healthy control subjects, recruited from a single center, with each PAH subject recruited simultaneously with a cohabitating non-PAH control subject. Shotgun metagenomic sequencing was used to analyze the microbiome profiles. There were no differences between PAH and non-PAH subjects across several measures of microbial abundance and diversity (Alpha Diversity, Beta Diversity, F/B ratio). The relative abundance of Lachnospiraceae bacterium GAM79 was lower in PAH stool samples as compared to non-PAH control subject' stool. There was no strong or reproducible association between PAH disease severity and global microbial abundance, but several bacterial species (a relative abundance of Anaerostipes rhamnosivorans and a relative deficiency of Amedibacterium intestinale, Ruminococcus bicirculans, and Ruminococcus albus species were associated with disease severity (most proximal right heart catheterization hemodynamics and six-minute walk test distance) in PAH subjects. Our results support further investigation into the presence, significance, and potential physiologic effects of a PAH-specific intestinal microbiome.

Keywords: clinical studies; diet; lung disease; microbial molecular genetics; obesity.

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Conflict of interest statement

The authors declare that there are no conflict of interests.

Figures

Figure 1
Figure 1
Flow of patients throughout the study. PAH, pulmonary arterial hypertension
Figure 2
Figure 2
Intestinal microbiota diversity measures between groups. (a) Distribution of observed species read counts. (b) Alpha Diversity (Shannon Index) between PAH and non‐PAH control groups. (c) Beta diversity principal component plot between PAH and non‐PAH control groups. (d) Firmicutes/bacteriodetes ratio between PAH and non‐PAH control groups. PAH, pulmonary arterial hypertension
Figure 3
Figure 3
Volcano plot of differential species abundance between PAH and non‐PAH control groups. FC, fold change; PAH, pulmonary arterial hypertension; PVR, pulmonary vascular resistance
Figure 4
Figure 4
Dot Plot representation of significant differential species abundance in relation to disease severity metrics in PAH group. (a) Significant bacterial species by PVR > 5 Wood units. (b) Significant bacterial species by six‐minute walk distance. (c) Significant bacterial species by mPAP. *Bacterial species (Anaerostipes rhamnosivorans, Amedibacterium intestinale, Ruminococcus bicirculans, and Ruminococcus albus) significant across all three metrics of disease severity. FC, fold change; PAH, pulmonary arterial hypertension; PVR, pulmonary vascular resistance
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